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Mechanism of early light signaling by the carboxy-terminal output module of Arabidopsis phytochrome B

ABSTRACT: Phytochromes are evolutionarily conserved photoreceptors in bacteria, fungi, and plants. The prototypical phytochrome comprises an N-terminal photosensory module and a C-terminal histidine kinase signaling-output module. However, the plant phytochrome has been postulated to transduce light signals by interacting with a group of nodal Phytochrome-Interacting transcription Factors (PIFs) and triggering their degradation via the N-terminal photosensory module, while its C-terminal output module, including a Histidine Kinase-Related Domain (HKRD), is thought not to participate directly in signaling. Here, we show that the C-terminal module of Arabidopsis phytochrome B (PHYB) is unexpectedly sufficient to mediate the degradation of PIF3 and to induce a distinct set of PIF-regulated photosynthetic genes. These signaling functions require the HKRD and particularly its dimerization. A D1040V mutation, which disrupts the dimerization of HKRD and the interaction between the C-terminal module and PIF3, abrogates the early light signaling functions of PHYB in nuclear accumulation, photobody biogenesis, and PIF3 degradation. In contrast, disruption of the interaction between PIF3 and PHYB’s N-terminal photosensory module has little effect on PIF3 degradation. Together, this study provides novel insight into the central mechanism of early phytochrome signaling that the C-terminal signaling-output module of PHYB interacts with PIF3 in the nucleus to mediate PIF3 degradation by light.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE90925 | GEO | 2017/12/31

SECONDARY ACCESSION(S): PRJNA356373

REPOSITORIES: GEO

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Arabidopsis thaliana

Project description:Mechanism of early light signaling by the carboxy-terminal output module of Arabidopsis phytochrome B

| PRJNA356373 | ENA

Transcriptome analysis of gene expression divergence in BBX11 mutation in red light

Project description:phytochrome B (phyB) acts as the red light photoreceptor and negatively regulates the growth-promoting factor PHYTOCHROME INTERACTING 4 (PIF4) through a direct physical interaction, which in turn changes the expression of a large number of genes. phyB-PIF4 module regulates a variety of biological and developmental processes in plants. In this study, we demonstrate that B-BOX PROTEIN 11 (BBX11) physically interacts with both phyB and PIF4. BBX11 negatively regulates PIF4 accumulation as well as its biochemical activity, consequently leading to the repression of PIF4-controlled genes' expression and promotion of photomorphogenesis in the prolonged red light. This study reveals a regulatory mechanism that mediates red light signal transduction and sheds a light on phyB-PIF4 module in promoting red light-dependent photomorphognenesis.

2022-11-02 | GSE166109 | GEO

Genome-wide identification of microRNAs and their targets involved in the phyB-mediated light signaling pathway in rice

Project description:Phytochrome B (phyB), one member of phytochrome family in rice, plays important roles in regulating a range of developmental processes, and stress responses. However, little information about the mechanism involved in phyB-mediated light signaling pathway has been reported in rice. Another, it has been well-known that microRNAs (miRNAs) perform important roles in plant development and stress responses. Thus it is intriguing to explore the role of miRNAs in phyB-mediated light signaling pathway in rice. In this study, comparative high-throughput sequencing and degradome analysis were adopted to identify candidate miRNAs and their targets that participate in phyB-mediated light signaling pathway. A total of 838 known miRNAs, 663 novel miRNAs and 1,957 target genes were identified from wild-type (WT) and phyB mutant. Among them, 135 miRNAs showed differential expression, suggesting that the expressions of these miRNAs are under the control of phyB. In addition, 32 out of the 135 differentially expressed miRNAs were detected to slice 70 genes in rice genome. Analysis of these target genes showed that members of various transcription factor families constitute the largest proportion, indicating miRNAs are probably involved in phyB-mediated light signaling pathway mainly via regulating the expression of transcription factors. This study presented a comprehensive expression analysis of miRNAs and their targets that might be involved in phyB-mediated light signaling pathway for the first time. The results provide new clues for functional characterization of miRNAs in phyB-mediated light signaling pathway, which would be helpful in comprehensively uncovering molecular mechanism of phytochrome-mediated photomorphogenesis and stress responses in plant. Examination of miRNA profiles in wild type (WT) and phyB mutant at four-leaf stage by deep sequencing using Illumina Hiseq2500.

2015-01-01 | E-GEOD-62334 | biostudies-arrayexpress

FERONIA regulates plant growth and survival under salt stress by modulating the dark reversion of phyB via a signature of phosphorylation

Project description:Here we report that FERONIA (FER) integrates phyB-mediated light signaling pathway to control salt stress response. Mutation in phytochrome B (phyB) largely suppresses the dwarfism and leaf bleaching phenotype of fer-4 mutant under salt stress. FER interacts with and phosphorylates the N-terminal domain of phyB. Mutation in fer-4 or disruption of the FER-mediated phosphorylation sites of phyB at Ser106 and Ser227 leads to a retention of phyB in the photobodies under dark conditions, suggesting that FER-mediated phosphorylation accelerates the dark reversion of phyB. Interestingly, salt stress slows down the dark reversion of phyB via the inhibition of the kinase activity of FER, and mutation of phyB or overexpression of PIF5 attenuates the salt-induced growth inhibition. Together, our study indicates that the plasma membrane-localized FER determines the dark reversion rate of phyB in the nucleus via a signature of phosphorylation and thus coordinates the extracellular stress signals and nuclear outputs to dynamically control plant growth and survival under stress conditions.

2021-11-08 | GSE188335 | GEO

Genome-wide identification of microRNAs and their targets involved in the phyB-mediated light signaling pathway in rice

2015-01-01 | GSE62334 | GEO

Genome-wide identification of PIF3-binding sites and direct-target genes of PIF3 transcriptional regulation in skotomorphogenesis [ChIP-Seq]

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF3 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis. Four biological replicates data of PIF3-binding sites were collected by comparing the parallel ChIP samples from transgenic seedlings overexpressing Myc-epitope-tagged PIF3 (35S:PIF3-5xMyc, P3M) in pif3-3 null mutant background and the wild-type (WT) control.

2013-02-01 | E-GEOD-39215 | biostudies-arrayexpress

RNA-seq Transcriptome Profiling of Tiller Buds in the First Leaf Axil of Phytochrome B mutant (phyB-1) and Wild-type Sorghum from Initiation to Dormancy (phyB-1) and Outgrowth (wild-type)

Project description:Phytochrome B (phyB) enables plants to modify shoot branching or tillering in response to varying light intensities and ratios of red and far-red light caused by shading and neighbor proximity. Tillering is inhibited in sorghum genotypes that lack phytochrome B (58M, phyB-1) until after floral initiation. The growth of tiller buds in the first leaf axil of wild-type (100M, PHYB) and phyB-1 sorghum genotypes is similar until 6 d after planting when buds of phyB-1 arrest growth, while wild-type buds continue growing and develop into tillers. Transcriptome analysis at this early stage of bud development identified numerous genes that were up to 50-fold differentially expressed in wild-type/phyB-1 buds. Up-regulation of terminal flower1, GA2oxidase, and TPPI could protect axillary meristems in phyB-1 from precocious floral induction and decrease bud sensitivity to sugar signals. After bud growth arrest in phyB-1, expression of dormancy-associated genes such as DRM1, GT1, AF1, and CKX1 increased and ENOD93, ACCoxidase, ARR3/6/9, CGA1, and SHY2 decreased. Continued bud outgrowth in wild-type was correlated with increased expression of genes encoding a SWEET transporter and cell wall invertases. The SWEET transporter may facilitate Suc unloading from the phloem to the apoplast where cell wall invertases generate monosaccharides for uptake and utilization to sustain bud outgrowth. Elevated expression of these genes was correlated with higher levels of cytokinin/ sugar signaling in growing buds of wild-type plants.

2017-03-30 | GSE79389 | GEO

Analyses of phyB-regulated genes by RNA-seq

Project description:The phytochrome family consists of five numbers (phyA-phyE) in Arabidopsis, of which phyB is the best characterized and shown to play a major role in mediating red light inhibition of hypocotyl elongation. In order to reveal the molecular basis for phyB-mediated red light signaling to promote photomorphogenesis, we analyzed the gene expression profile of red light-grown WT and phyB mutant seedlings by high throughput sequencing.

2020-07-25 | GSE101875 | GEO

Phytochrome B photobodies are comprised of phytochrome B and its primary and secondary interacting proteins

Project description:Phytochrome B (phyB) is a plant photoreceptor that forms a membraneless organelle called a photobody. However, its constituents are not fully known. Here, we isolated phyB photobodies from Arabidopsis leaves using fluorescence-activated particle sorting and analyzed their components. We found that a photobody comprises ~1,500 phyB dimers along with other proteins that could be classified into two groups: The first includes proteins that directly interact with phyB and localize to the photobody when expressed in protoplasts, while the second includes proteins that interact with the first group proteins and require co-expression of a first-group protein to localize to the photobody. As an example of the second group, TOPLESS (TPL) interacts with PHOTOPERIODIC CONTROL OF HYPOCOTYL 1 (PCH1) and localizes to the photobody when co-expressed with PCH1. Mutations in TPL family members cause shortened hypocotyls under red light, demonstrating that the method identifies photobody components that regulate red light signaling. Together, our results support that phyB photobodies include not only phyB and its primary interacting proteins but also its secondary interacting proteins.

2023-04-03 | PXD040702 | Pride

Expression data from epidermis specific phytochrome B or global phytochrome B line comparing to phyB-9 mutant.

Project description:Seedling hypocotyls display negative gravitropism in the dark but agravitropism in the light. The Arabidopsis thaliana pif quadruple mutant (pifQ), which lacks four PHYTOCHROME-INTERACTING FACTORS (PIFs), is agravitropic in the dark. Endodermis-specific expression of PIF1 rescues gravitropism in pifQ mutant seedlings. Since phytochromes induce light responses by inhibiting PIFs and the COP1-SPA ubiquitin E3 ligase complex in the nucleus, we asked whether phyB can cell autonomously inhibit hypocotyl negative gravitropism in the endodermis. We found that while epidermis-specific expression of PHYB rescues hypocotyl negative gravitropism and all other phyB mutant phenotypes, endodermis-specific expression of PHYB does not. Epidermal phyB induces the phosphorylation and degradation of endodermal PIFs in response to red light. This induces a global gene expression pattern similar to that induced by red light treatment of seedlings expressing PHYB under the control of its own endogenous promoter. Our results imply that epidermal phyB generates an unidentified mobile signal that travels to the endodermis where it promotes PIF degradation and inhibits hypocotyl negative gravitropism.

2017-02-08 | GSE87591 | GEO

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